Enhanced Rate Capability and Cycle Performance of Titanium-Substituted P2-Type Na0.67Fe0.5Mn0.5O2 as a Cathode for Sodium-Ion Batteries.

In this study, we developed a doping technology capable of improving the electrochemical performance, including the rate capability and cycling stability, of P2-type Na0.67Fe0.5Mn0.5O2 as a cathode material for sodium-ion batteries. Our approach involved using titanium as a doping element to partly substitute either Fe or Mn in Na0.67Fe0.5Mn0.5O2. The Ti-substituted Na0.67Fe0.5Mn0.5O2 shows superior electrochemical properties compared to the pristine sample. We investigated the changes in the crystal structure, surface chemistry, and particle morphology caused by Ti doping and correlated these changes to the improved performance. The enhanced rate capability and cycling stability were attributed to the enlargement of the NaO2 slab in the crystal structure because of Ti doping. This promoted Na-ion diffusion and prevented the phase transition from the P2 to the OP4/″Z″ structure.

Effects of exercise on mature or precursor brain­derived neurotrophic factor pathways in ovariectomized rats.

Ovariectomy (OVX) is a method used to block estrogen in female rats that induces hippocampal dysfunction and affects brain­derived neurotrophic factor (BDNF) pathways. The majority of previous studies investigating OVX focused on BDNF expression in the hippocampus and cognitive function. The present study focused on the pathways of each BDNF type, precursor (proBDNF) and mature (mBDNF), and the effects of regular exercise in the hippocampus of ovariectomized rats. Female Sprague­Dawely rats were used and OVX surgery was performed. After 1 week of recovery from surgery, two groups of rats that received OVX surgery were subjected to regular treadmill exercise for 8 weeks. The results of protein levels by western blotting indicated that the expression of proBDNF, p75 neurotrophin receptor (p75NTR) and c­Jun N­terminal protein kinase (JNK) was increased, and mBDNF, tropomyosin­related kinase B (TrkB) and nuclear factor­κB expression was significantly reduced in the OVX control group compared with the sham control group SC (P<0.05). Thus, the survival pathway by mBDNF was impaired and the pro­apoptotic response was activated by increased JNK expression due to proBDNF­p75NTR binding in the hippocampus of ovariectomized rats. By contrast, exercise reduced activation of the pro­apoptotic response and increased mBDNF­TrkB expression in the hippocampus of ovariectomized rats. Thus, regular exercise may increase the activation of survival pathways via mBDNF and reducing the activation of the pro­apoptotic pathway of proBDNF in the hippocampus of ovariectomized rats.

Voluntary wheel running ameliorates symptoms of MK-801-induced schizophrenia in mice.

Schizophrenia is a chronic and severe mental disorder characterized by the disintegration of cognitive thought processes and emotional responses. Despite the precise cause of schizophrenia remains unclear, it is hypothesized that a dysregulation of the N­methyl­D­aspartate (NMDA) receptor in the brain is a major contributing factor to its development. Brain­derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is implicated in learning and memory processes. In the present study, we investigated in vivo the effects of voluntary wheel running on behavioral symptoms associated with NMDA receptor expression, using MK­801­induced schizophrenic mice. Abilify (aripiprazole), a drug used to treat human schizophrenia patients, was used as the positive control. For the assessment of behavioral symptoms affecting locomotion, social interaction and spatial working memory, the open­field, social interaction and Morris water maze tests were conducted. For investigating the biochemical parameters, NMDA receptor expression in the hippocampal CA2­3 regions and prefrontal cortex was detected by NMDA immunofluorescence and BDNF expression in the hippocampus was measured using western blot analysis. MK­801 injection for 14 days induced schizophrenia­like behavioral abnormalities with decreased expression of the NMDA receptor and BDNF in the brains of mice. The results indicated that free access to voluntary wheel running for 2 weeks alleviated schizophrenia­like behavioral abnormalities and increased the expression of NMDA receptor and BDNF, comparable to the effects of aripiprazole treatment. In the present study, the results suggest that NMDA receptor hypofunctioning induced schizophrenia­like behaviors, and that voluntary wheel running was effective in reducing these symptoms by increasing NMDA receptor and BDNF expression, resulting in an improvement of disease related behavioral deficits.

Chiropractic approach on genu varum.

Bowed legs adjustment should first, follow careful biomechanical examination of left and right side per its range of motion may differ respectively. Adjustment should be applied according to the findings of the biomechanical tests. Bowed legs can be defined as the result of restriction of joints, excluding the pathological joint problems.

Treadmill exercise enhances NMDA receptor expression in schizophrenia mice.

Schizophrenia is a serious psychiatric disorder with several symptoms including cognitive dysfunction. Although the causes of schizophrenia are still unclear, there is a strong suspicion that the abnormality in N-methyl-D-aspartate (NMDA) receptor may contribute to schizophrenia symptoms. In the present study, the effect of treadmill exercise on the NMDA receptor expression was evaluated using MK-801-induced schizophrenia mice. Immunohistochemistry for expressions of NMDA receptor tyrosine hydroxylase (TH) was conducted. Western blot for brain-derived neurotrophic factor (BDNF) was also performed. In the present results, the mice in the MK-801-treated group displayed reduced NMDA receptor expression. Enhanced TH expression and suppressed BDNF expression were also observed in the MK-801-treated mice. Treadmill exercise improved NMDA receptor expression in the MK-801-induced schizophrenia mice. Treadmill exercise also suppressed TH expression and enhanced BDNF expression in the MK-801-induced schizophrenia mice. The present study showed that down-regulation of NMDA receptor demonstrated schizophrenia-like parameters, meanwhile treadmill running improved schizophrenia-related parameters through enhancing NMDA receptor expression.

Treadmill exercise exerts ameliorating effect on isolation-induced depression via neuronal activation.

Maternal isolation has been used as a valid animal model of early life stress, and it induces depression to offspring. Exercise ameliorates the incidence and severity of stress-related mood disorders, such as depression and anxiety. Here in this study, we investigated the effects of treadmill exercise on brain neuronal excitation in the rat pups with maternal isolation-induced depression. Forced swimming test and immunohistochemistry for glucocorticoid receptor and c-Fos in the hippocampal dentate gyrus and hypothalamic paraventricular nucleus were conducted. Maternal isolation lasted for 6 hours per day and was continued from postnatal day 1 to postnatal day 30. The rat pups in the exercise group were forced to run on a treadmill for 30 min once a day for 10 consecutive days, starting from the postnatal day 21 until the postnatal day 30. In the present results, treadmill exercise alleviated depressive state in the maternal separated rat pups, as potently as fluoxetine treatment. Treadmill exercise also restored the expressions of glucocorticoid receptor and c-Fos in the hippocampal dentate gyrus and hypothalamic paraventricular nucleus of the maternal separated rat pups near to the control level, as fluoxetine treatment. The present study suggests the possibility that treadmill exercise can be used as the therapeutic strategy for the childhood depression induced by disturbed mother-child relationship.

Treadmill exercise alleviates prenatal noise stress-induced impairment of spatial learning ability through enhancing hippocampal neurogenesis in rat pups.

Stress alters brain cell properties and then disturbs cognitive processes, such as learning and memory. In this study, we investigated the effect of postnatal treadmill exercise on hippocampal neurogenesis and spatial learning ability of rat pups following prenatal noise stress. The impact of exercise intensity (mild-intensity exercise vs heavy-intensity exercise) was also compared. The pregnant rats in the stress-applied group were exposed to a 95 dB supersonic machine sound for 1 h once a day from the 15th day after mating until delivery. After birth, the rat pups in the exercise groups were made to run on a treadmill for 30 min once a day for 7 consecutive days, starting 4 weeks after birth. The spatial learning ability was tested using radial-arm maze task and hippocampal neurogenesis was determined by 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry. The rat pups born from the stress-applied maternal rats spent more time for the seeking of water and showed higher number of error in the radial-arm maze task compared to the control group. These rat pups showed suppressed neurogenesis in the hippocampus. In contrast, the rat pups performed postnatal treadmill exercise saved time for seeking of water and showed lower number of error compared to the stress-applied group. Postnatal treadmill exercise also enhanced neurogenesis in the hippocampus. The mild-intensity exercise showed more potent impact compared to the heavy-intensity exercise. The present results reveal that postnatal treadmill exercise lessens prenatal stress-induced deterioration of brain function in offspring.

Short-term treadmill exercise preserves sensory-motor function through inhibiting apoptosis in the hippocampus of hypoxic ischemia injury rat pups.

Perinatal hypoxic ischemia injury is a common cause of morbidity and mortality in neonates. Physical exercise may ameliorate neurological impairment by impeding neuronal loss following various brain insults. In the present study, the effect of treadmill exercise on sensory-motor function in relation with hippocampal apoptosis following hypoxic ischemia brain injury was investigated. Sensory-motor function was determined by walking initiation test and apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and caspase-3 immunohistochemistry. On postnatal 7 day, left common carotid artery of the neonatal rats was ligated for two hours and then the neonatal rats were exposed to hypoxia conditions for one hour. The rat pups in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 10 days, starting 22 days after induction of hypoxic ischemia brain injury. Hypoxic ischemia caused sensory-motor disturbance with enhancement of apoptosis in the hippocampus. Short-term treadmill exercise suppressed hypoxic ischemia injury-induced apoptosis in the hippocampus, and preserved sensory-motor function of hypoxic ischemia injury rat pups.

Treadmill exercise ameliorates motor disturbance through inhibition of apoptosis in the cerebellum of valproic acid-induced autistic rat pups.

Autism is a neurological disorder that occurs during childhood and is characterized by impairments in social interaction and communication, as well as restricted and repetitive behaviors. Abnormalities of the cerebellum in autism include Purkinje cell loss and motor disturbance. In the present study, we evaluated the effect of treadmill exercise on motor coordination and balance in correlation with reelin expression and the rate of apoptosis in the cerebellum of autistic rat pups. For the induction of the autism-like animal models, 400 mg/kg valproic acid was subcutaneously injected into rat pups on postnatal day 14. Rat pups in the exercise groups were forced to run on a treadmill for 30 min, once a day, five times a week for 4 weeks, starting on postnatal day 28. Motor coordination and balance, as measured using the rotarod test and vertical pole test, were affected by the induction of autism. By contrast, treadmill exercise ameliorated motor dysfunction in the autistic rat pups. The expression levels of reelin, GAD67 and cyclin D1 in the cerebellum of the autistic rat pups were decreased, while the expression levels of these molecules were increased in autistic rat pups who engaged in treadmill exercise. In the cerebellum of the autistic rat pups, Bcl-2 expression was decreased and Bax expression was increased. By contrast, treadmill exercise enhanced Bcl-2 expression and suppressed Bax expression. The therapeutic effect of treadmill exercise on motor deficits may be due to the reelin-mediated anti-apoptotic effect on cerebellar Purkinje neurons.